chapter 005 and 006 pathology
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Chapter 005 and 006 PathologyTRANSCRIPT
Chapter 5
Inflammation and Healing
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Review of Body Defenses
First line of defense Nonspecific Mechanical barrier Unbroken skin and mucous membranes Secretions such as tears and gastric juices
Second line of defense Nonspecific Phagocytosis Inflammation
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Review of Body Defenses(Cont.)
Third line of defense Specific defense Production of specific antibodies or cell-mediated
immunity
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Defense Mechanisms in the Body
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Normal Capillary Exchange
Generally not all capillaries in a particular capillary bed are open. Depend on the metabolic needs of the cells or
need of removal of wastes Movement of fluid, electrolytes, oxygen, and
nutrients on arterial end based on net hydrostatic pressure
Venous end—osmotic pressure will facilitate movement of fluid, carbon dioxide, and other wastes.
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Normal Capillary Exchange Versus Inflammatory Response
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Physiology of Inflammation
A protective mechanism and important basic concept in pathophysiology
Disorders are named using the ending –it is. Inflammation is a normal defense mechanism Signs and symptoms serve as warning for a
problem: Problem may be hidden within the body.
It is not the same as infection. Infection, however, is one cause of inflammation.
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Causes of Inflammation
Direct physical damage Examples: cut, sprain
Caustic chemicals Examples: acid, drain cleaner
Ischemia or infarction Allergic reactions Extremes of heat or cold Foreign bodies
Examples: splinter, glass Infection
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Steps of Inflammation
Injury to capillaries and tissue cells Release of bradykinin from injured cells Bradykinin stimulates pain receptors. Pain causes release of histamine. Bradykinin and histamine cause capillary
dilation. Break in skin allows bacteria to enter tissue Neutrophils phagocytize bacteria. Macrophages (mature monocytes) leave the
bloodstream and phagocytose microbes.
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Acute Inflammation
Process of inflammation is the same, regardless of cause.
Timing varies with specific cause Chemical mediators affect blood vessels and
nerves in the damaged area: Vasodilation Hyperemia Increase in capillary permeability Chemotaxis to attract cells of the immune system
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Chemical Mediators in the Inflammatory Response
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Local Effects of Inflammation
Redness and warmth Caused by increased blood flow to damaged area
Swelling (edema) Shift of protein and fluid into the interstitial space
Pain Increased pressure of fluid on nerves; release of
chemical mediators (e.g., bradykinins) Loss of function
May develop if cells lack nutrients; edema may interfere with movement.
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Exudate
Serous Watery, consists primarily of fluid, some proteins,
and white blood cells Fibrinous
Thick, sticky, high cell and fibrin content Purulent
Thick, yellow-green, contains more leukocytes, cell debris, and microorganisms
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Systemic Effects of Inflammation
Mild fever (pyrexia) Common if inflammation is extensive Release of pyrogens
Malaise Feeling unwell
Fatigue Headache Anorexia
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The Course of Fever
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Changes in the Blood with Inflammation
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Course of Inflammation and Healing
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Potential Complications of Inflammation
Infection Microorganisms can more easily penetrate
edematous tissues. Some microbes resist phagocytosis. The inflammatory exudate also provides an
excellent medium for microorganisms. Skeletal muscle spasm
May be initiated by inflammation Protective response to pain
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Chronic Inflammation
Follows acute episode of inflammation Less swelling and exudate Presence of more lymphocytes,
macrophages, and fibroblasts Continued tissue destruction More fibrous scar tissue Granuloma may develop around foreign
object
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Potential Complications
Deep ulcers may result from severe or prolonged inflammation Caused by cell necrosis and lack of cell
regeneration that causes erosion of the tissue • Can lead to complications such as perforation of viscera• Extensive scar tissue formation
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Treatment of Inflammation
Acetylsalicylic acid (ASA) Aspirin
Acetaminophen Tylenol
Nonsteroidal anti-inflammatory drugs (NSAIDs) Ibuprofen
Glucocorticoids Corticosteroids
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Drugs Used to Treat Inflammation
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Anti-Inflammatory Effects of Glucocorticoids
Decreased capillary permeability Enhanced effectiveness of epinephrine and
norepinephrine Reduced number of leukocytes and mast
cells Reduces immune response
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Adverse Effects of Glucocorticoids
Atrophy of lymphoid tissue; reduced hemopoiesis Increased risk of infection
Catabolic effects Increased tissue breakdown; decreased protein
synthesis Delayed healing Delayed growth in children Retention of sodium and water because of
aldosterone-like affect in the kidney
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“RICE” Therapy for Injuries
Rest Ice Compression Elevation
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Types of Healing
Resolution Minimal tissue damage
Regeneration Damaged tissue replaced with cells that are
functional Replacement
Functional tissue replaced by scar tissue Loss of function
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The Healing Process
Healing of incised wound by first intention
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The Healing Process (Cont.)
Healing by second intention
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Scar Formation
Loss of function Result of loss of normal cells and specialized
structures• Hair follicles• Nerves• Receptors
Contractures and obstructions Scar tissue is nonelastic. Can restrict range of movement
Adhesions Bands of scar tissue joining two surfaces that are
normally separated
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Scar Formation (Cont.)
Hypertrophic scar tissue Overgrowth of fibrous tissue
• Leads to hard ridges of scar tissue or keloid formation
Ulceration Blood supply may be impaired around scar
• Results in further tissue breakdown and ulceration at future time
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Complications of Scar Tissue
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Complications of Scar Tissue (Cont.)
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Burns
Thermal—caused by flames or hot fluids Chemical Radiation Electricity Light Friction
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Classification of Burns
Superficial partial-thickness (first-degree) burns Involve epidermis and part of dermis Little, if any, blister formation
Deep partial-thickness (second-degree) burns Epidermis and part of dermis Blister formation
Full-thickness (third- and fourth-degree) burns Destruction of all skin layers and often underlying
tissues
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Classification of Burn Injury by Depth
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Examples of Burns
Partial-thickness burn
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Examples of Burns (Cont.)
Deep partial-thickness burn
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Examples of Burns (Cont.)
Full-thickness burn
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Effects of Burn Injury
Both local and systemic Dehydration and edema Shock Respiratory problems Pain Infection Increased metabolic needs for healing period
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Assessment of Burn Area Using the Rule of Nines
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Healing of Burns
Hypermetabolism occurs during healing period.
Immediate covering of a clean wound is needed to prevent infection.
Healing is a prolonged process. Scar tissue develops, even with skin grafting. Physiotherapy and occupational therapy may
be necessary. Surgery may be necessary to release
restrictive scar tissue.
Chapter 6
Infection
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Microorganisms
Small living forms Include bacteria, fungi, protozoa, viruses Many can grow in artificial culture medium Nonpathogenic
Usually do not cause disease unless conditions change
Part of normal flora Often beneficial
Pathogens Disease-causing microbes
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Types of Microorganisms
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Bacteria
Classified as prokaryotes No nuclear membrane—no nucleus Function metabolically and reproduce Divide by binary fission Complex cell wall structure Do not require living tissues to survive Vary in size and shape
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Reproduction by Binary Fission
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Major Groups of Bacteria
Bacilli Rod-shaped organisms
Spirochetes Include spiral forms and Vibrio spp.
Cocci Spherical forms
• Diplococci• Streptococci• Staphylococci
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Basic Structure of Bacteria
Rigid cell wall Protects and provides a specific shape Two types that differ in chemical composition:
• Gram-positive• Gram-negative
Useful in selecting appropriate antimicrobial therapy
Cell membrane located inside the bacterial cell wall Selectively permeable
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Structure of a Bacterium and Mode of Action of Antimicrobial Drugs
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Basic Structure of Bacteria (Cont.)
External capsule or slime layer Found in some Outside the cell wall Offers additional protection
Flagellae One or more attached to cell wall Provide motility for some species
Pili or fimbriae Tiny hairlike structures—found in some bacteria Assist in attachment to tissue Transfer of DNA to another bacterium
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Basic Structure of Bacteria (Cont.)
Cell membrane Inside the bacterial cell wall Selectively permeable
Cytoplasm contains: Chromosome
• One long strand of DNA Ribosomes and RNA Plasmids
• DNA fragments; nonchromosomal; exchange DNA during conjugation
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Basic Structure of Bacteria (Cont.)
Toxins Exotoxins
• Usually produced by gram-positive bacteria Endotoxins
• Present in the cell wall of gram-negative bacteria• Released on death of bacterium• Vasoactive compounds that can cause septic shock
Enzymes • Damage tissues and promote spread of infection
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Spore Formation
Spores Formed by several species Dormant-latent form of bacterium Can survive long periods of time in spore state Highly resistant to heat and disinfectants
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Viruses
Small obligate intercellular parasites Protein coat or capsid Protein coat comes in various shapes and
sizes Can change (mutate) quickly
Nucleic acid DNA or RNA Classification dependent on nucleic acid present Some RNA-containing viruses contain reverse
transcriptase enzyme to convert RNA to DNA.
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Different Shapes of Viruses
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Active Viral Infection
Virus attaches to host cell. Viral genetic material enters the cell. Viral DNA or RNA takes control of cell. Uses host’s cell to synthesize viral proteins
and nucleic acids New viruses are assembled in cytoplasm of
cell. Viruses released by lysis of host cell or by
budding from host cell membrane
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Viral Replication
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Latent Viral Infection
Virus enters cell as with active infection. Viral proteins are produced and Inserted into
membrane of the host cell. This may stimulate an immune response and destruction of host cell.
Virus may reproduce actively if immune system is depressed (e.g., herpesviruses)
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Chlamydia, Rickettsiae, Mycoplasmas
Obligate intercellular parasites. Do not grow on artificial media Some similarities with both bacteria and
viruses Lack some basic components Classified as bacteria Replicate by binary fission within host cell
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Chlamydia, Rickettsiae, Mycoplasmas (Cont.)
Chlamydia Common cause of sexually transmitted disease Can result in infertility
Rickettsiae Gram-negative Transmitted by insect vectors (lice, ticks)
Mycoplasmas Lack cell wall Cause of atypical type pneumonia
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Fungi
Eukaryotic organisms (contain nucleus) Found throughout environment
On animals, plants, humans, food Fungal or mycotic infection
From single-celled yeast or multicellular molds Only a few are pathogenic.
Cause primary infection on skin or mucous membranes but may spread systemically particularly in immunosuppressed individual
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Examples of Fungal Diseases
Histoplasma can cause neurologic disease and can be transmitted to embryo or fetus if mother is infected
Tinea pedis (athlete’s foot) Candida: usually harmless, but opportunistic
Causative agent of thrush and vaginitis Pneumocystis jirovecii
Opportunistic organism causing pneumonia Has some characteristics of fungi and some of
protozoa
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Protozoa
Eukaryotic forms Unicellular, lack cell wall Many live independently, others are obligate
parasites Pathogens are usually parasites. Examples of protozoal diseases:
Trichomoniasis Malaria Amebic dysentery
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Other Agents of Disease
Helminths (flatworms or roundworms) Are not microorganisms Parasites May be small or up to 1 m in length Life cycle with at least three stages
• Ovum, larva, adult Enter body through skin or by ingestion,
depending on species Infections more commonly found in young children Infection can be life-threatening in an
immunosuppressed client.
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Helminth Diseases
Pinworms: ova inhaled in dust in fecally contaminated areas; common in children worldwide
Hookworms: larvae enter skin from fecally contaminated soil in tropical areas
Tapeworms: most common form transmitted by larvae in undercooked pork
Ascaris—giant roundworm: ingested with food that has been grown in feces-contaminated soil or prepared with hands that have been in feces-contaminated soil
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Other Agents of Disease (Cont.)
Prions Protein-like agents that change the shape of
proteins within host cells Transmitted by contaminated tissues
• Ingestion of meat • Infected blood or donor organs
Cause degenerative disease of the nervous system
Human prion diseases• Creutzfeldt-Jacob disease and variant Creutzfeldt-Jacob
disease• Both rapidly progressive and fatal
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Resident Flora
Many areas of the body have a resident population of mixed microorganisms termed normal flora. Skin Nasal cavity Mouth Gut Vagina Urethra
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Principles of Infection
Infection—organism is able to reproduce in or on body’s tissues
Sporadic In a single individual
Endemic Continuous transmission within a population
Epidemic Higher than normal transmission or spread to new
geographical area Pandemic
Transmission has occurred on most continents.
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Transmission of Infectious Agents
Transmission from person to person Reservoir
Source of infection Person with active infection Person who is asymptomatic
Carrier A person may never develop the disease but still
is a carrier. A person with subclinical signs of the disease
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Transmission of Infectious Agents: Links in the Infection Chain
Agent: the microbe causing the infection Reservoir:
Environmental source such as contaminated soil Infected person or animal
• Person may carry the agent and show no signs of disease
• Person or animal may show signs and symptoms of disease
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Transmission of Infectious Agents: Links in the Infection Chain (Cont.)
Portal of exit: means whereby the agent leaves the reservoir
Mode of transmission: method whereby the agent reaches a new susceptible host Air Water Direct contact Food
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Transmission of Infectious Agents: Links in the Infection Chain (Cont.)
Portal of entry: access to new host Susceptible host: susceptibility will depend
on: Health status Immunity Age Nutrition
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Transmission of Infectious Agents
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Modes of Transmission
Direct contact No intermediary Touching infectious lesion, sexual activity Contact with infected blood or bodily secretions
Indirect contact Involves intermediary object or organism Contaminated hand or food Fomite—inanimate object
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Modes of Transmission (Cont.)
Droplet transmission Respiratory or salivary secretions are expelled
from infected individual Aerosol transmission
Involve small particles from the respiratory tract Suspended in air and can travel farther than
droplets Vector-borne
Insect or animal is an intermediate host
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Nosocomial Infections
Occur in health care facilities Hospitals, nursing homes, physician’s offices,
dental offices 10% to 15% of patients acquire an infection in
the hospital because of: Many microbes present Patients with undiagnosed infectious disease Shared environment Treatment that may cause weakened immune
system Many health care workers and fomites act as
reservoirs.
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Host Resistance and Microbial Virulence
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Factors That Decrease Host Resistance
Age (infants and older adults) Pregnancy Genetic susceptibility Immunodeficiency Malnutrition Chronic disease Severe physical or emotional stress Inflammation or trauma Impaired inflammatory responses
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Virulence and Pathogenicity
Pathogenicity Capability of a microbe to cause disease
Virulence Degree of pathogenicity
• Invasive qualities (e.g., motility or enzymes)• Toxins • Adherence to tissue by pili, fimbriae, specific receptor
sites• Ability to avoid host defenses
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New Issues Affecting Infection and Transmission
Newly emerging diseases Antigenetically different forms of common
infections such as influenza Spread beyond normal endemic areas
Superinfections Multidrug-resistant forms of existing diseases
• TB• Staphylococcus aureus
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Control of Transmission and Infection
Infection control requires two approaches: Standard Precautions used in all settings with all
clients when body fluids may be exchanged. Specific Precautions in clients diagnosed with a
particular infection—these are used in addition to standard precautions.
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Infection Cycle and Breaking the Chain
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Break the Cycle: Provide an Example of Each of the Actions
Locate and remove or isolate the reservoir of infection.
Identify and restrict access to contaminated food or water.
Reduce contact between infected persons and the remainder of the population.
Block portals of exit and entry. Remove or block modes of transmission. Reduce host susceptibility by immunizations,
adequate nutrition, and access to health care.
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Additional Techniques to Reduce Transmission
Adequate cleaning of surroundings and clothing
Sterilization Disinfectants Antiseptics
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Physiology of Infection
Incubation period Time between entry of organism into the body and
appearance of clinical signs of disease Vary considerable with different organisms
Prodromal period Fatigue, loss of appetite, headache Nonspecific—“coming down with something” More evident in some infections than others
Acute period Infectious disease develops fully
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Means of Disinfection
Sterilization of equipment by: Chemicals Heat in an autoclave NOTE: Equipment must be cleaned prior to
sterilization or it will remain contaminated! Use of chemicals:
Antiseptics are used on the skin and tissues. Disinfectants are used on surfaces or objects.
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Patterns of Infection
Local infections Focal infections Systemic infections
Septicemia Bacteremia Toxemia Viremia
Mixed infections Primary infections Secondary infections, subclinical infections
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Causes and Development
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Signs and Symptoms of Infection
Local signs of inflammation Pain, swelling, redness, warmth
• If bacterial—purulent exudate• If viral—serous, clear exudate
Systemic signs of inflammation Fever may be present. Fatigue and weakness Headache Nausea
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Methods of Diagnosis
Culture and staining techniques Using specific clinical specimens Drug sensitivity tests
Blood tests Variations in numbers of leukocytes
• Leukocytosis—bacterial infection• Leukopenia—viral infection
Differential count C-reactive protein Erythrocyte sedimentation rate (ESR)
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Diagnostic Tests (Cont.)
Immunological testing of body fluids Antigen identification Antibody titer
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Guidelines for Drug Therapy
Drugs should be administered and taken as directed. Antimicrobial drugs should be taken until prescribed
medication is completely used or until new drug is prescribed.
If symptoms continue without reduction, contact the pharmacist or physician.
Do not use drugs prescribed for other clients or other infections.
If drug resistance is known to occur with infection, use multidrug therapy.
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Classification of Antimicrobials
Antibiotic Drugs derived from organisms
Antimicrobial Antibacterial Antiviral Antifungal
Bactericidal Drugs destroy organism
Bacteriostatic Decrease rate of reproduction
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Classification of Antimicrobials (Cont.)
Broad spectrum Effective against both gram-positive and gram-
negative organisms Narrow spectrum
Effective against either gram-positive or gram-negative organisms
First- and second-generation drugs First generation—original drug class Second generation—later version, which may be
more effective, more tolerable, or more easily administered
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Mode of Action of Antibiotics
Interfere with bacterial cell wall synthesis Example: penicillin
Increase permeability of bacterial cell membrane Example: polymyxin
Interfere with protein synthesis Example: tetracycline
Interfere with synthesis of essential metabolites Example: sulfonamides
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Mode of Action of Antivirals
Drugs may act by: Blocking entry into host cell Inhibiting gene expression Inhibiting assembly of the virus
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Antifungal Agents
May interfere with mitosis in fungi May increase fungal membrane permeability Most antifungal agents administered topically
to skin or mucous membranes Fungi are eukaryotic cells and are therefore
often toxic to animal and human cells. Treatment requires strict medical supervision.
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Antiprotozoal agents
Similar characteristics to antifungal agents Protozoans are eukaryotic cells. Many pathogenic protozoa have several
stages in their life cycles. Require treatment with different agents at different
stages of the cycles